Gentilini A, Caligiuri A, Provenzano A, Marra F
Department of Experimental and Clinical Medicine, University of Florence, Largo Brambilla, 3, I50134 Florence, Italy.
Curr Mol Med. 2016;16(8):710-720. doi: 10.2174/1566524016666161021163252.
Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease, characterized by inflammation, hepatocyte injury and fibrogenesis. Overall mortality, and liver-related mortality, are both increased in NASH patients. Considering that nonalcoholic fatty liver disease is the most prevalent hepatic abnormality in the Western world, understanding the mechanisms leading to NASH and its progression to cirrhosis is critical for a better management of these patients. Moreover, a more detailed knowledge of this condition may be helpful to identify those subjects which are more susceptible to develop progressive liver disease. Emerging data indicate that NASH progression results from parallel events originating from the liver as well as from the adipose tissue, and the gastrointestinal tract. In this review we highlight some of the most recent findings reported on the pathogenesis of NASH and its fibrogenic progression to cirrhosis, in an effort to identify possible targets for treatment or biomarkers of disease progression.
非酒精性脂肪性肝炎（NASH）是一种非酒精性脂肪性肝病的进展形式，其特征为炎症、肝细胞损伤和纤维化。NASH患者的总体死亡率以及与肝脏相关的死亡率均有所增加。鉴于非酒精性脂肪性肝病是西方世界最普遍的肝脏异常情况，了解导致NASH及其进展为肝硬化的机制对于更好地管理这些患者至关重要。此外，对这种病症更详细的了解可能有助于识别那些更容易发展为进行性肝病的个体。新出现的数据表明，NASH的进展源于肝脏、脂肪组织以及胃肠道同时发生的事件。在本综述中，我们重点介绍了关于NASH发病机制及其纤维化进展为肝硬化的一些最新研究发现，以期确定可能的治疗靶点或疾病进展的生物标志物。
